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SMP - MNE Exam 2 > Lecture 25: Diabetes Insipidus Case > Flashcards

Lecture 25: Diabetes Insipidus Case Flashcards

1
Q

What is the normal serum [Na+]?

A

135-145 mE/L

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2
Q

What are the 5 types of diabetes insipidus (3 names for first one and 2 for second one)?

A
  1. Central = neurogenic = hypothalamic
  2. Nephrogenic = renal
  3. Gestational
  4. Dipsogenic
  5. Psychogenic
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3
Q

What is central/neurogenic diabetes insipidus due to? Overall and 4 main causes by order of incidence?

A

Inability to synthesize or secrete active vasopressin due to:

  1. Hypothalamic lesions (40-50% of cases) due to tumor, sarcoidosis, or histiocytosis (langerhan’s cell)
  2. Neurosurgery damaging neurons around the base of the brain
  3. Idiopathic (20-30% of cases) due to autoimmune inflammatory attack on posterior pituitary = lymphocytic infundibuloneurohypophysitis
  4. Genetics (5% of cases)
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4
Q

What is nephrogenic diabetes insipidus due to? What can cause this (4 potential causes (2 types))?

A 
Inability of kidney to detect vasopressin
Causes:
1. Familial:
- V2 mutation: X-linked recessive
- AQP2 mutation: autosomal dominant
2. Acquired:
- Hypercalcemia (above 13)
- Hypokalemia (below 2.5)
- Drugs: lithium, demeclocycline
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5
Q

What is gestational diabetes insipidus due to?

A

Placenta secretes vasopressinase that degrades vasopressin

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6
Q

What is diabetes insipidus characterized by?

A

Large dilute urine volume

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7
Q

What are the 4 possible diseases that can cause polyuria?

A
  1. Osmotic diuresis
  2. Diabetes insipidus
  3. Primary polydipsia
  4. Osmoreceptor dysfunction
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8
Q

What is osmotic diuresis caused by? Example? Blood osmolarity?

A

Osmotic agent in the urine causing excessive urination
Eg: glucose in diabetics
Normal blood osmolarity because thirst regulation is intact

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9
Q

What are the 2 types of primary polydipsia?

A
  1. Dipsogenic DI

2. Psychogenic DI

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10
Q

What is the most common cause of polyruria in Western countried?

A

Primary polydipsia

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11
Q

What does polydipsia mean?

A

Excessive water intake

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12
Q

What is dipsogenic DI? 4 causes?

A

Low thirst threshold caused by:

  1. Mass lesions in posterior pituitary
  2. Granulomatous diseases: inherited primary immunodeficiency disease which increase the body’s susceptibility to infections caused by certain bacteria and fungi: masses of immune cells that form at sites of infection or inflammation
  3. Aging
  4. Idiopathic
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13
Q

What is psychogenic DI?

A

Excessive drinking due to psychiatric disorders or simply believing it’s more healthy, not actual thirst

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14
Q

Describe osmoreceptor dysfunction. Blood concentration?

A

Osmoreceptors connected to and regulating AVP secretion and thirst have lesions or are destroyed so you are lacking AVP AND THIRST
Hyperosmolar blood

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15
Q

What is DI’s incidence?

A

1 in 10-15,000 people

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16
Q

What % of DI compared to DM?

A

0.1%

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17
Q

Has the DI incidence increased over the past 50 years?

A

NOPE

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18
Q

What are the 2 types of body fluid homeostasis?

A
  1. Osmotic

2. Volume

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19
Q

What is the normal range of blood osmolality?

A

280-295 mOsm/kg

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20
Q

What is the definition of osmolality?

A

Solute (mOsm) / water (kg)

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21
Q

What does total plasma osmolality primarily include? How do their concentrations relate to one another?

A
  1. Na+
  2. H2CO3-
  3. Cl-

[Na+] = [H2CO3-] + [Cl-]

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22
Q

What is the equation to calculate plasma osmolality?

A

Plasma osmolality = 2 x[Na+] + glucose (mg/dL)/18 + BUN (mg/dL)/2.8

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23
Q

What does BUN stand for?

A

Blood urea Nitrogen

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24
Q

What is the effective osmotic pressure?

A

The osmolality of the impermeable particles that contribute to the osmotic pressure

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25
Q

What is the equation to calculate effective plasma osmolality?

A

Effective plasma osmolality = 2 x[Na+] + glucose (mg/dL)/18

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26
Q

Why is BUN not included in the equation for effective plasma osmolality?

A

Because nitrogen can freely diffuse through plasma membranes

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27
Q

Describe the genes that encode for AVP.

A

Genes encode a large precursor hormone, vasotocin, and the 9 AA at the N-terminal is AVP
The rest is secreted into the blood and has no biological effect

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28
Q

What are the 5 regulators of AVP secretion by hypo?

A
  1. Blood hyperosmolality
  2. Angiotensin II
  3. Decreased atrial receptor firing = hypovolemia = increased AVP secretion
  4. Sympathetic stimulation
  5. Hypervolemia sensed by baroreceptors and natriuretic peptide in the brain: inhibition of AVP secretion
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29
Q

What 2 hypo nuclei is AVP secreted by?

A
  1. Paraventricular

2. Supraoptic

30
Q

What is the role of ADH?

A

Reabsorption of water in kidney tubules to decrease plasma osmolality and concentrate urine

31
Q

What are the 3 vasopressin receptors?

A
  1. Vasopressin V2
  2. Vasopressin V1a
  3. Vasopressin V1b
32
Q

Where is Vasopressin V2 located? How does it work?

A

Location: kidney (distal and collecting tubules)

Allows for vasopressin to function as ADH to reabsorb water

33
Q

Where is Vasopressin V1a located? How does it work?

A

Location: smooth muscle, CNS, liver

Causes vasoconstriction

34
Q

How do the osmoreceptor afferent magnocellular neurons detect high blood osmolality? How sensitive are they?

A

When body is hyperosmolar the fenestrations of hypo let solute go through, this shrinks the cells that have fenestrations and activates the magnocellular neurons
VERY sensitive: respond to changes in osmolality of less than 1%

35
Q

How would you characterize the osmotic regulation of vasopressin secretion?

A

Linear: increases as osmolality increases AT ANY BP!

36
Q

Describe the 8 steps that happens when vasopressin binds the V2 receptors? What is this process referred to as?

A
  1. Vasopressin binds V2 on basolateral membrane
  2. Binding releases GDP from the Gs part of the receptor and GTP binds instead
  3. Gs bound to GTP binds to adenylyl cyclase to activate it
  4. cAMP synthesis
  5. Protein kinase A activation
  6. Phosphorylation of vesicles in cytoplasm that contain aquaporins (AQP-2)
  7. Insertion of aquaporins into apical/luminal membrane to reabsorb water
  8. Water pumped back into the cell (because collecting duct cell medium is always hyperosmolar) and then interstitial space via the AQP3 and 4 aquaporins of the basolateral membrane

ANTIDIURESIS

37
Q

Where is Vasopressin V1b located? How does it work?

A

Location: corticotrophs of ant pit

Works with CRH to release ACTH

38
Q

What is sarcoidosis

A

The growth of tiny collections of inflammatory cells in different parts of the body.

39
Q

What is histiocytosis?

A

Abnormal increase in the number of immune cells

40
Q

Can pituitary lesions cause DI?

A

Usually not but can decrease the amount of secreted ADH

41
Q

How can central DI be confirmed with an MRI? 2 ways

A
  1. Swelling of the pituitary stalk on an MRI = central DI due to idiopathic cause: lymphocytic infundibuloneurohypophysitis
  2. No pituitary seen on an MRI (no bright spot)
42
Q

How common is central DI compared to other DI types?

A

Rare: less than 1:25,000

43
Q

Which is more rare: central or nephrogenic DI?

A

Nephrogenic

44
Q

How can we SCREEN for DI?

A

ALL criteria for hypotonic polyuria must be met:

  1. 24 hr urine volume > 50 mL/kg under conditions of ad lib intake
  2. Urine specific gravity below 1.010 OR Uosm below 300 mOsm/kg
  3. Absence of osmotic diuresis (dipstick test for glucose negative)
45
Q

What does ad lib mean in medicine?

A

At one’s own pleasure, desire

46
Q

In what patients with polyuria do you see normal blood osmolarity and BP and why?

A
  1. Osmotic diuresis
  2. Central DI
  3. Nephrogenic DI
  4. Gestational DI
    Because their thirst is intact and regulates blood osmolarity and BP
47
Q

What are 2 tests to diagnose DI?

A
  1. Overnight outpatient test: patient withholds drinking from after dinner until morning and plasma [Na+] and Uosm is measured: if below 800 (or even 600) mOsm DI is ruled out
  2. Formal inpatient test: patient withholds drinking until body weight decreases by 3-5% OR until osmolality plateaus quickly OR until [Na+] is above 145 mmol/L. THEN: measure Uosm: if below 300 then DI!
    To determine which DI type:
    administer AVP
    - If Uosm increases by more than 50% = central DI
    - If Uosm increases by less than 10% = nephrogenic DI
    - Intermediate results: inconclusive
48
Q

How common is gestational DI?

A

Rare

49
Q

What are 5 symptoms of hypovolemia?

A
  1. Orthostatic dizziness: blood pressure falls significantly when you stand up quickly
  2. Tachychardia: rapid heart rate
  3. Hypotension
  4. Syncope: temporary loss of consciousness caused by a fall in blood pressure
  5. Death
50
Q

Hypovolemia vs hypotension?

A

Hypovolemia is low blood volume while hypotension is low blood pressure

51
Q

What are 9 symptoms of hyperosmolarity?

A
  1. Dry mouth
  2. Thirst
  3. Decreased sweating
  4. Lethargy
  5. Disorientation
  6. Obtundation: less than full alertness
  7. Coma
  8. Venous thrombosis (deep vein, pulmonary embolism, stroke)
  9. Death
52
Q

Why can DI patients have a poor quality of life?

A

Cause they need to drink and pee all the time

53
Q

Treatments for DI? How do they work?

A
  1. Water
  2. Antidiuretic agents (for central DI only):
    - AVP
    - Desmopressin (DDAVP): AVP analog 2/3 times/day either orally or intranasally
54
Q

How does DDAVP differ from AVP? What is their purpose?

A

D-Arg instead of L-Arg at position 8 and amino group removed from N-terminal => much longer half-life than AVP and does not stimulate V1a receptors

55
Q

What are the 2 major defenses for maintenance of osmotic homeostasis?

A
  1. AVP (neural and renal)

2. Thirst (neural)

56
Q

What does AVP stand for?

A

Arginine vasopressin

57
Q

What is diuresis?

A

Collecting duct is impermeable to water (normal state)

58
Q

What is psychosis-intermittent hyponatremia-polydipsia (PIP) syndrom?

A

Increased fluid intake by schizophrenic patients: type of psychogenic DI

59
Q

How do we make a DI diagnosis?

A

Patient has to be shown to excrete a hypotonic urine despite the presence of a hyperosmolar serum (aka when the patient is dehydrated)

60
Q

How do patients with partial central DI respond to the formal water deprivation test?

A

Their urine concentrate a little (but not until 1000 mosm/kg like in normal people) because they secrete a little AVP, just not enough. Giving them AVP will work.

61
Q

How do patients with primary polydipsia respond to the formal water deprivation test?

A

Their urine concentrate a little (but not until 1000 mosm/kg like in normal people) and they do not respond to AVP

62
Q

How else can we differentiate central DI from nephrogenic DI? When is this usually done?

A

Measure plasma AVP when blood is hyperosmolar (dehydrated)

Usually done after a formal water deprivation test

63
Q

Explain how hyperosmolarity affect the brain. Why do we have to be very careful when fixing hyperosmolar patients?

A

High osmolality = shrinking of the brain = brain adapts by accumulating electrolytes and organic osmolytes

If you fix it too rapidly it will cause cerebral edema

64
Q

When do patients with DI experience symptoms of hyperosmolarity and hypovolemia?

A

When they cannot drink in response to thirst

65
Q

Why do people with DI prefer cold water?

A

Cold water better quenches thirst

66
Q

Would you ever confuse a DI patient with an osmoreceptor dysfunction patient?

A

NOPE because the osmoreceptor dysfunction patient has no thirst

67
Q

What does wanting COLD water mean?

A

Means someone has TRUE thirst

68
Q

Is diabetes insipidus associated with obesity?

A

NOPE

69
Q

What blood cells line the collecting duct cells?

A

Vasa recta

70
Q

How can central DI be confirmed with a biopsy?

A

Post pit will show T-cells which means it’s idiopathic central DI

71
Q

How come DDAVP can be administered orally or intranasally even though it’s a peptide?

A

It’s protected from degradation

SMP - MNE Exam 2 (17 decks)

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